|
Diabetes mellitus complications affect all system of body including gut.
Gut manifestations can be grouped as follows
a) Due to autonomic neuropathy.
b) In the presence of G.I. involvement, management of diabetes mellitus may be
difficult.
c) Gut hormones play a role in release of insulin normally. This aspect may be
impaired in NIDDM.
Oral manifestation of diabetes mellitus are periodontitis and diffuse alveolar atrophy, diabetes mellitus may be diagnosed by dentist because of these changes.
Oesophagus shows motility disorder. There is diminished primary peristalsis and tertiary waves are prominent. Occasionally dilated oesophagus is seen. These are caused due to vasculopathy and autonomic neuropathy. Clinical manifestations are subtle. In diabetes mellitus lower gastro oesophageal sphincter tone is reduced leading to reflux oesophagitis. Clinically presenting as retosternal burning. Insulin: glucagon ratio is altered in uncontrolled diabetes mellitus. Increase glucagon level lowers the LES sphincter tone.
Changes in stomach
There is delayed in gastric emptying. This situation is known as gastro paresis diabeticorum. Clinically it manifests as anorexia, epigastric fullness after eating. There is intermittent vomiting.
Gastric splash may be elicited even after 6-8 hours of eating. Because of delayed gastric emptying absorption of food and oral hypoglycemic agents may be erratic leading to brittle diabetes characterised by frequent hypoglycemia and hyperglycemia. The gastic atony in diabetes mellitus is due to autonomic neuropathy, probably due to diminished vagal tone or due to autovagotomy. Increased glucagon levels in diabetes mellitus may inhibit gastro
intestinal motility.
Hel secretion is diminished in diabetes mellitus. This is due to chronic atrophic gastritis. In IDDM, there is association of parietal cell antibodies and intrinsic factor antibodies. This is because of autoimmune mechanism. Incidence of gastric ulcer is increased while incidence of duodenal ulcer is decreased when compared to nondiabetic population.
During the episodes of diabetic ketoacidosis gastric atony occurs and there is dilated stomach. This is due to the effect of acidosis and hyperglycemia. Gut symptoms of DKA are well known like nausea, vomiting, abdominal pain and anorexia.
Serum gastrin level is increased in diabetes. This state is described as pseudo Zollinger Ellison syndrome. This is due to vagal denervation and due to functional gastric outlet obstruction as a result of gastric atony.
Diabetic diarrhoea occurs in long duration IDDM and NIDDM. Often it is accompanied by peripheral neuropathy, autonomic neuropathy, nephropathy and retinopathy. Diarrhoea is marked in nights. It is watery. It is secretory diarrhoea- It shows remission and exacerbation. In the past, it was treated by B12 injection and clonidine. Erythromycin and other G.I. prokinetic drugs are quite effective. Symptomatic treatment can be done by loperamide and codeine.
Diabetics can also have steatorrhoea particularly in fibrocalculous pancreatic diabetes. This is due to associated pancreatic exocrine deficiency. It responds to pancreatic enzyme replacement and restriction of fat.
Bacterial overgrowth in a intestinal dilated, atonic loop leads to conjugation of bile salts resulting in steatorrhoea.
Constipation can occur in an uncontrolled diabetes mellitus due to dehydration state. More common in elderly with poor roughage intake. Long standing diabetes mellitus may have a mega sigmoid colon with atony as a result of autonomic neuropathy. At times patients on metformin have constipation.
Perianal skin may be affected by moniliasis in uncontrolled diabetes mellitus.
Liver and diabetes mellitus
Cirrhosis may be associated with diabetes mellitus or it can occasionally caused by haemochromatosis. Incidence of haemochromatosis was reported in 16 cases out of 10,000 diabetics studied at Joslin Clinic.1
While treating diabetes mellitus with cirrhosis caution should be used in using oral hypoglycemic agents. As they are not metabolised, half-life is increased and with long acting antidiabetic drugs, hypoglycemia results. Hence one will prefer to use short acting hypoglycemic drugs like tolbutamide. Avoid using phenformin particularly because lactic acidosis often occurs as this drug has to be metabolised through liver. Use of chlorpropamide is avoided as there is risk of cholestatic jaundice.
In patient with lupoid hepatitis and diabetes mellitus steroid therapy is used and this may aggrevate hyperglycaemia. Cirrhosis patients show in their plasma increase in insulin level due to poor degradation of insulin by liver. Neoglucogenesis and glycogenolysis occur at a slower phase due to diseased liver. Hence they will show mild fasting hyperglycemia and marked 2 Hr. postprandial hyperglycemia.
Hepatic glucokinase levels are decreased and glucose-6-phosphate and fructose- 6- phosphate levels are increased in diabetics with cirrhosis.
When viral hepatitis occurs in diabetes mellitus there is prolonged cholestasis and morbidity. Hepatomegaly is often seen in uncontrolled diabetes mellitus. This is partly due to.fatty liver and partly due to glycogen infiltration of liver. During diabetic ketoacidosis liver is enlarged and tender.
In diabetes, liver functions are usually normal. Pancreatitis when it occurs in diabetes mellitus often precipitates diabetic ketoacidosis. Pancreatic classification with exocrine function disturbance is seen in fibrocalculus pancreatic diabetes mellitus.
Elderly persons may develop for the first time diabetes mellitus with migratory thrombophlebitis due to cancer of pancreas.
Gall bladder disease and diabetes mellitus2
Gall bladder disease has more serious prognosis in diabetics than non diabetic. Incidence of gallstones in diabetes mellitus is approximately 25% as compared to 8% in non diabetic population. Plan for elective surgery in diabetics with cholelithiasis and cholecystitis. Gall bladder dysfunction described as the diabetic neurogenic gall bladder is characterised by a large size gall bladder with poor concentration of dye after a fatty meal. Biliary dyskinesia, emphysematous cholecystitis are more common in the diabetics.
Entero insulin axis
It is well observed phenomenon that when glucose is orally given, there is greater plasma insulin rise compared to intravenous glucose administration. This phenomenon is attributed to gut hormones which have facilitatory effect on insulin release. Two gut hormones namely glucose dependent, insulin peptide and glucagon like peptide hormone are released in response to nutrients. Glucagon like peptide hormone stimulates release of insulin from beta cells.3 It also Simulates somato-statin while it suppresses glucagon release. Glucose dependant insulin peptide has lesser stimulatory effect. Loss of responsivity to glucose like peptide-I may be an important component of the abnormal glucose homeostasis that characterises NIDDM. In patients with NIDDM the effect to augment insulin secretion by GLP-I is reduced or lost. GLP-I or its structurally modified analogue may be used in the treatment of NIDDM. It is desirable to treat patients with NIDDM with an agent that stimulates endogenous insulin by subcutaneous injection because endogenous insulin is delivered to the liver through the portal blood flow rather than from the systemic circulation. GLP-I provide potential advantages over the commonly used sulfonylurea as a treatment for NIDDM. Insulinotropic action of GLP-I unlike those of the sulfonylurea are regulated by plasma glucose concentrations. In human subjects the relative potential of GLP-I action on its receptor is atenuated as the glucose falls below 90 mgm/dl where as all actions are absent at glucose levels less than 50 mgm/dl. By contrast sulphonylurea induced insulin secretion continues regardless of ambient glucose concentration, hence hypoglycemia is not anticipated with GLP-I
REFERENCES
1. William K. Jenson - The digestive system and diabetes' in Joselin's D.M., Allyander
Marble. Priseilla White, Robert F. Bradlay Chapter 27, 12th Edition Lea & Febiger
Philadelphia 1994.
2. Dr. Manchandra - Diabetes & Digestive system in New Mediwave published by Lupin
Lab. Page. 125.
3. Potential of Glucagon like peptide in persons with diabetes. Diabetes in the XXI
century Nobles florisa part I March 246-26, 1994.
|
